Abstract
Objective To study the activation of alveolar macrophage β (AM) and the expression of co-stimulatory molecule CD40 in transfusion-related acute lung injury (TRALI) model in order to illustrate the pathogenesis of TRALI. Methods Sixty SD rats were randomly (random number) divided into normal control group (n=15) with sham operation using normal saline instead of LPS and plasma, positive control group (n=15) with ALI induced by intravenous infusion of 5 mg/kg lipopolysaccharide (LPS) in equivalent volume of whole blood drawn out) , and TRALI group (n=15) treated by intra-peritoneal injection of 2 mg/kg LPS 2 h before the transfusion of human plasma (1 mL whole blood about 10% of total blood volume drawn out and replaced with 1 mL plasma) , LPS control group (n=15) treated by intra-peritoneal injection of 2 mg/kg LPS 2 h before saline infusion in equivalent volume of blood drawn out. The pathologic changes of rat lung tissue were observed by HE staining. The expression of TLR4 was examined by RT-PCR. The activation of NF-кB in AM was measured by electrophoresis mobility shift assay (EMSA). The expression of CD40 mRNA and CD40 molecule were analyzed by Northern blot and flow cytometry respectively. ELISA was performed to detect the concentration of TNF-α, MIP-2 and IL-1β in broncho-alveolar lavage fluid (BALF). Results Broken alveolar septa, hyperemia, and massive infiltration of inflammatory cells including the neutrophils were observed in lung tissues of TRALI group. The expression of TLR4 gene was detected in activated macrophage phi (AMφ) of TRALI group rats. The activation of NF-кB was increased in TRALI group rats. The expression of CD40 in AMφ was higher in rats of TRALI group than that in rats of control group and LPS control group. The concentration of TNF-α, MIP-2 and IL-1β were enhanced significantly in BALF of TRALI group rats. Conclusion The activation of AM and up-regulation of co-stimulatory molecule CD40 induced release of some inflammatory cytokines. It suggested that AM activation may play an important role in the pathogenesis of TRALI. Key words: Acute lung injury; Macrophage; TLR4; CD4 molecule
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